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Viral hepatitis

Viral hepatitis
Micrograph showing ground glass hepatocytes, which are seen in chronic hepatitis B infections (a type of viral hepatitis), and represent accumulations of viral antigen in the endoplasmic reticulum. H&E stain.
Classification and external resources
ICD-10 B15–B19
ICD-9-CM 070
MeSH D006525

Viral hepatitis is liver inflammation due to a viral infection.[1] It may present in acute (recent infection, relatively rapid onset) or chronic forms. The most common causes of viral hepatitis are the five unrelated hepatotropic viruses Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E. In addition to the nominal hepatitis viruses, other viruses that can also cause liver inflammation include Herpes simplex, Cytomegalovirus, Epstein–Barr virus, and Yellow fever.


  • Hepatitis viruses 1
    • Hepatitis A 1.1
    • Hepatitis B 1.2
    • Hepatitis C 1.3
    • Hepatitis D 1.4
    • Hepatitis E 1.5
    • Hepatitis F virus 1.6
    • GB virus C 1.7
  • Other viruses 2
  • References 3

Hepatitis viruses

The most common cause of hepatitis is viral. Although they are classified under the disease hepatitis, these viruses are not all related.

Hepatitis viruses
Transmission Enteral Parenteral Parenteral Parenteral Enteral
Classification Picornavirus Orthohepadnavirus Hepacivirus Deltavirus Hepevirus
Genome +ssRNA dsDNA-RT +ssRNA −ssRNA +ssRNA
Antigens HBsAg,HBeAg Core antigen Delta antigen
Incubation period 20–40 days 45–160 days 15–150 days 30–60 days 15–60 days
Severity/Chronicity[2] mild; acute occasionally severe; 5–10% chronic subclinical; 70% chronic exacerbates symptoms of HBV; chronic w/ HBV normal patients, mild; pregnant women, severe; acute
Vaccine 10 year protection 3 injections, lifetime protection None available None available Investigational (approved in China)

Hepatitis A

Hepatitis A or infectious jaundice is caused by hepatitis A virus (HAV), a picornavirus transmitted by the fecal-oral route often associated with ingestion of contaminated food. It causes an acute form of hepatitis and does not have a chronic stage. The patient's immune system makes antibodies against HAV that confer immunity against future infection. People with hepatitis A are advised to rest, stay hydrated and avoid alcohol. A vaccine is available that will prevent HAV infection for up to 10 years. Hepatitis A can be spread through personal contact, consumption of raw sea food or drinking contaminated water. This occurs primarily in third world countries. Strict personal hygiene and the avoidance of raw and unpeeled foods can help prevent an infection. Infected people excrete HAV with their feces two weeks before and one week after the appearance of jaundice. The time between the infection and the start of the illness averages 28 days (ranging from 15 to 50 days),[3] and most recover fully within 2 months, although approximately 15% of sufferers may experience continuous or relapsing symptoms from six months to a year following initial diagnosis.[4]

Hepatitis A[5]
Marker Detection Time Description Significance
Faecal HAV 2–4 weeks or 28days Early detection
Ig M anti HAV 4–12 weeks Enzyme immunoassay for antibodies During Acute Illness
Ig G anti HAV 5 weeks – persistent Enzyme immunoassay for antibodies Old infection or Reinfection

Hepatitis B

Hepatitis B is caused by hepatitis B virus, a hepadnavirus that can cause both acute and chronic hepatitis. Chronic hepatitis develops in the 15% of adults who are unable to eliminate the virus after an initial infection. Identified methods of transmission include blood (blood transfusion, now rare), unsanitary tattoos, sexually (through sexual intercourse or through contact with blood or bodily fluids), or via mother to child by breast feeding (minimal evidence of transplacental crossing). However, in about half of cases the source of infection cannot be determined. Blood contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor blades, or touching wounds on infected persons. Needle-exchange programmes have been created in many countries as a form of prevention.

Patients with chronic hepatitis B have antibodies against hepatitis B, but these antibodies are not enough to clear the infection of the affected liver cells. The continued production of virus combined with antibodies is a likely cause of the immune complex disease seen in these patients. A vaccine is available that will prevent infection from hepatitis B for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths per year worldwide due to the complications of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Hepatitis B is endemic in a number of (mainly South-East Asian) countries, making cirrhosis and hepatocellular carcinoma big killers. There are six treatment options approved by the U.S. Food and Drug Administration (FDA) available for persons with a chronic hepatitis B infection: alpha-interferon, pegylated interferon, adefovir, entecavir, telbivudine and lamivudine. About 65% of persons on treatment achieve a sustained response.

Hepatitis C

Hepatitis C (originally "non-A non-B hepatitis") is caused by hepatitis C virus (HCV), an RNA virus that is a member of the Flaviviridae family. HCV can be transmitted through contact with blood (including through sexual contact if the two parties' blood is mixed) and can also cross the placenta. Hepatitis C usually leads to chronic hepatitis, culminating in cirrhosis in some people. It usually remains asymptomatic for decades. Patients with hepatitis C are susceptible to severe hepatitis if they contract either hepatitis A or B, so all persons with hepatitis C should be immunized against hepatitis A and hepatitis B if they are not already immune, and avoid alcohol. HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drug ribavirin. The genotype of the virus is the primary determinant of the rate of response to this treatment regimen, with genotype 1 being the most resistant.

Hepatitis C is the most common chronic blood-borne infection in the United States.[6]

Hepatitis C[7]
Marker Detection Time Description Significance Note
HCV-RNA 1–3 weeks or 21 days PCR Demonstrates presence or absence of virus Results may be intermittent during course of infection. Negative result is not indicative of absence.
anti-HCV 5–6 weeks Enzyme Immunoassay for antibodies Demonstrates past or present infection High false positive in those with autoimmune disorders and populations with low virus prevalence.
ALT 5–6 weeks Peak in ALT coincides with peak in anti-HCV Fluctuating ALT levels is an indication of active liver disease.

Hepatitis D

The Hepatitis D virus (HDV) or hepatitis delta agent is similar to a viroid as it can only propagate in the presence of the hepatitis B virus.

Hepatitis E

The Hepatitis E virus (HEV), from the Hepeviridae family, produces symptoms similar to hepatitis A, although it can take a fulminant course in some patients, particularly pregnant women; chronic infections may occur in immune-compromised patients. It is more prevalent in the Indian subcontinent.

Hepatitis F virus

Hepatitis F virus (HFV) is a hypothetical virus linked to hepatitis. Several hepatitis F virus candidates emerged in the 1990s; none of these reports have been substantiated.

GB virus C

The GB virus C is another potential viral cause of hepatitis that is probably spread by blood and sexual contact.[8] It was initially identified as Hepatitis G virus.[9] There is very little evidence that this virus causes hepatitis, as it does not appear to replicate primarily in the liver.[10] It is now classified as GB virus C.[11]

Other viruses

The first virus capable of causing hepatitis was the yellow fever virus a mosquito borne flavivirus. Other viruses than can cause hepatitis include:

KIs-V is a virus isolated in 2011 from four patients with raised serum alanine transferases without other known cause. A causal role is suspected.[20]


  1. ^ National Library of Medicine » Medical Subject Headings »Virus Diseases (C02) » Hepatitis, Viral, Human (C02.440) » Scope Note. 
  2. ^ Kuo, Infectious Causes of Jaundice, ATSU School of Osteopathic Medicine Arizona, June 2012
  3. ^ "CDC Hepatitis A FAQ". Retrieved 2008-03-03. 
  4. ^ "CDC Hepatitis A Fact Sheet". Retrieved 2008-03-03. 
  5. ^ "Acute Viral Hepatitis : Introduction Harrison's Principle of Internal Medicine, 17 Edition". 
  6. ^ "CDC DVH—Hepatitis C Information For the Health Professional". Retrieved 2010-01-14. 
  7. ^ "WHO | Hepatitis C". 2010-12-08. Retrieved 2012-08-26. 
  8. ^ Stark J; et al. (1996). "Detection of the hepatitis G virus genome among injecting drug users, homosexual and bisexual men, and blood donors". J. Infect. Dis. 174 (6): 1320–3.  
  9. ^ Linnen J, Wages J, Zhang-Keck ZY; et al. (1996). "Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent". Science 271 (5248): 505–8.  
  10. ^ Pessoa MG, Terrault NA, Detmer J; et al. (1998). "Quantitation of hepatitis G and C viruses in the liver: evidence that hepatitis G virus is not hepatotropic". Hepatology 27 (3): 877–80.  
  11. ^ "00.026. Flaviviridae". ICTVdB Index of Viruses. 
  12. ^ Miguet JP, Coaquette A, Bresson-Hadni S, Lab M; Coaquette; Bresson-Hadni; Lab (June 1990). "[The other types of viral hepatitis]". Rev Prat (in French) 40 (18): 1656–9.  
  13. ^ Chau TN, Lee KC, Yao H; et al. (February 2004). "SARS-associated viral hepatitis caused by a novel coronavirus: report of three cases". Hepatology 39 (2): 302–10.  
  14. ^ Naides SJ (May 1998). "Rheumatic manifestations of parvovirus B19 infection". Rheum. Dis. Clin. North Am. 24 (2): 375–401.  
  15. ^ Xiong W (November 2010). "[Clinical efficacy of treating infant cytomegalovirus hepatitis with ganciclovir and impact on cytokines]". Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi (in Chinese) 26 (11): 1130–2.  
  16. ^ Okano M, Gross TG; Gross (November 2011). "Acute or Chronic Life-Threatening Diseases Associated With Epstein-Barr Virus Infection". Am. J. Med. Sci. 343 (6): 483–9.  
  17. ^ Anderson, D.R.; Schwartz, J.; Hunter, N.J.; Cottrill, C.; Bissaccia, E.; Klainer, A.S. (1994). "Varicella Hepatitis: A Fatal Case in a Previously Healthy, Immunocompetent Adult". Archives of Internal Medicine (JAMA) 154 (18): 2101–2106.  
  18. ^ Gallegos-Orozco JF, Rakela-Brödner J; Rakela-Brödner (October 2010). "Hepatitis viruses: not always what it seems to be". Rev Med Chil 138 (10): 1302–11.  
  19. ^ Papic N, Pangercic A, Vargovic M, Barsic B, Vince A, Kuzman I; Pangercic; Vargovic; Barsic; Vince; Kuzman (September 2011). "Liver involvement during influenza infection: perspective on the 2009 influenza pandemic". Influenza Other Respi Viruses 6 (3): e2–5.  
  20. ^ Satoh K, Iwata-Takakura A, Osada N; et al. (October 2011). "Novel DNA sequence isolated from blood donors with high transaminase levels". Hepatol. Res. 41 (10): 971–81.  
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